Regulation of autophagy by ROS: physiology and pathology.
By R. Scherz-Shouval, Zvulun Elazar. TIBS -Trends in Biochemical Sciences. Regular ed, 2011
1,246 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6234fa0392ea34b28c8d378488a72c14f4c7268a
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Citations in the corpus
- Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress☆ (2017, background): “hagy [63,64], mitophagy [65] and cell death in the forms of apoptosis, ferroptosis and necroptosis [66].”
- Zinc oxide nanoparticles induce oxidative DNA damage and ROS-triggered mitochondria mediated apoptosis in human liver cells (HepG2) (2012, background): “ROS also inhibit ATG4 protease activity, thereby supporting autophagosome formation [56].”
- Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines (2018, background): “Dysfunctional mitochondria seem to be able to initiate an auto-feedback loop to increase autophagy, so that damaged mitochondria or misfolded proteins are degraded which reduces inflammasome activation and risk of further tissue injury, though this system is less efficient in aging (141).”
- The dynamic nature of autophagy in cancer. (2011, background): “Additionally, the overexpression of p62 as a result of autophagy inhibition was shown to be important in the promotion of tumorigenesis through a variety of mechanisms, including deregulation of NF-kB signaling, accumulation of ROS, and increased DNA damage (Mathew et al. 2009). p62 contains a UBA d”
- Role of nrf2 in oxidative stress and toxicity. (2013, background): “Autophagy is accompanied by accumulation of ROS from damaged mitochondria (87).”
- Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “Two genes, which encode the OMM kinase PINK1 and the E3 ubiquitin ligase parkin, are mutated in autosomal recessive Parkinson’s disease [140].”
- Beta Cell Dysfunction and Insulin Resistance (2013, background): “Beta cells are highly dependent on ATP production for GSIS and are vulnerable to excess ROS because of their inherently low expression of antioxidant enzymes (Simmons, 2007).”
- Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis (2012, methodology): “The experiment labeled ‘‘4 C’’ assayed the binding of WT and Atg5fl/flLysmCre+/ apoptotic macrophages to WT macrophages (mean ± SEM; *p < 0.01). mitophagy (Scherz-Shouval and Elazar, 2011).”